| First Author | Belyaeva OV | Year | 2018 |
| Journal | J Biol Chem | Volume | 293 |
| Issue | 18 | Pages | 6996-7007 |
| PubMed ID | 29567832 | Mgi Jnum | J:263879 |
| Mgi Id | MGI:6189614 | Doi | 10.1074/jbc.RA117.001646 |
| Citation | Belyaeva OV, et al. (2018) Retinol dehydrogenase 11 is essential for the maintenance of retinol homeostasis in liver and testis in mice. J Biol Chem 293(18):6996-7007 |
| abstractText | Retinol dehydrogenase 11 (RDH11) is a microsomal short-chain dehydrogenase/reductase that recognizes all-trans- and cis-retinoids as substrates and prefers NADPH as a cofactor. Previous work has suggested that RDH11 contributes to the oxidation of 11-cis-retinol to 11-cis-retinaldehyde during the visual cycle in the eye's retinal pigment epithelium. However, the role of RDH11 in metabolism of all-trans-retinoids remains obscure. Here, we report that microsomes isolated from the testes and livers of Rdh11(-/-) mice fed a regular diet exhibited a 3- and 1.7-fold lower rate of all-trans-retinaldehyde conversion to all-trans-retinol, respectively, than the microsomes of WT littermates. Testes and livers of Rdh11(-/-) mice fed a vitamin A-deficient diet had approximately 35% lower levels of all-trans-retinol than those of WT mice. Furthermore, the conversion of beta-carotene to retinol via retinaldehyde as an intermediate appeared to be impaired in the testes of Rdh11(-/-)/retinol-binding protein 4(-/-)(Rbp4(-/-)) mice, which lack circulating holo RBP4 and rely on dietary supplementation with beta-carotene for maintenance of their retinoid stores. Together, these results indicate that in mouse testis and liver, RDH11 functions as an all-trans-retinaldehyde reductase essential for the maintenance of physiological levels of all-trans-retinol under reduced vitamin A availability. |
